Abstract
Human T-cell leukemia virus type 1 (HTLV-1) is the world’s first retrovirus with pathogenicity to cause adult T-cell leukemia-lymphoma (ATL) and chronic inflammatory diseases,such as HTLV-1 associated myelopathy/tropical spastic paraparesis (HAM/TSP) and HTLV-1 uveitis. As the virological characteristic, HTLV-1 can transmit efficiently only through cell-to-cell contact. Spread of infection and viral persistence is ingeniously driven by several viral genes as exemplified by HTLV-1 bZIP factor (HBZ) and tax. After the infection, the virus promotes proliferation and immortalization of the infected cells with acculturating immunophenotype into effector/memory T cells. In addition, HBZ enhances expression of co-inhibitory receptors on the surface of infected cells, potentially leading to suppression of host immune responses. These viral strategies can also result in unforeseen by-product, the pathogenicity of HTLV-1-associated diseases. In this review, with recent progress of HTLV-1 researches, we focus on astute regulation systems of the viral genes developed by HTLV-1.
